Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019829 (Hodgkin's disease)
 30,247 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Monoclonal antibody to Leu-M1, a granulocyte-related differentiation antigen, represents a highly effective reagent for detection of diagnostic Reed-Sternberg (R-S) cells and variants in paraffin-embedded tissues of Hodgkin's disease. In 69 of 73 cases of Hodgkin's disease (41 nodular sclerosis, 25 mixed cellularity, 4 lymphocyte predominance, and 3 lymphocyte depletion types), R-S cells were strongly immunoreactive for Leu-M1. Four cases of lymphocyte predominance Hodgkin's disease (nodular) were uniformly nonreactive for Leu-M1. In most of the positive cases (57/69, 83%), the majority (60-90%) of R-S cells and variants exhibited immunoreactivity for Leu-M1. A characteristic staining pattern included granular and/or vesicular cytoplasmic immunoreactivity, often with a prominent globular paranuclear reaction product, and membrane staining with highly irregular cytoplasmic borders. Evaluation of B-cell (37 specimens), T-cell (20 specimens), and true histiocytic (3 specimens) neoplasms and a case of mastocytosis revealed immunoreactivity for Leu-M1 only in 1 B-cell and 4 T-cell malignancies. The staining patterns in these cases, however, clearly differed from that observed for R-S cells. Studies of nonneoplastic lymphoid tissues (38 total) demonstrated that lymphoid cells were typically nonreactive; histiocytes revealed variable reactivity for Leu-M1. Occasional histiocytes of the sinusoidal network of lymph nodes, particularly in toxoplasmic lymphadenitis, exhibited a staining pattern (membranous/cytoplasmic/paranuclear) similar to that observed for R-S cells. Leu-M1 represents a potentially helpful diagnostic discriminant in the assessment of Hodgkin's disease and its distinction from non-Hodgkin's lymphomas and other lymphoid proliferations.
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PMID:Leu-M1--a marker for Reed-Sternberg cells in Hodgkin's disease. An immunoperoxidase study of paraffin-embedded tissues. 388 32

This report describes the phenotypic analysis of a cell line obtained from a female patient with the nodular sclerosing subtype of Hodgkin's disease (HD). The cell line has a neoplastic karyotype and is stable in culture in the absence of feeder layers or growth factors. Phenotypic analysis of this cell line shows that it cannot easily be characterized as either a lymphocyte, macrophage or granulocyte but resembles in its characteristics certain HD lines already described in the literature. The cell line carries the antigen defined by the Ki-1 monoclonal antibody, shows myeloid markers on a proportion of cells and has cytoplasmic UCH-T1.
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PMID:Phenotypic analysis of an established cell line derived from a patient with Hodgkin's disease (HD). 401 43

Two cases in adults with recurrent staphylococcal infections associated with abnormal granulocytic chemotaxis and hyperimmunoglobulinaemia E (Job's syndrome) are described. The pathophysiological mechanisms seems to consist of an abnormal IgE reaction against staphylococcal antigens causing secondary abnormality of granulocyte function. Abnormal cellular immune function was demonstrated in vitro and in vivo. Corticosteroid administration at first proved effective in both patients. One patient developed Hodgkin's disease of the mixed type in the course of the disease.
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PMID:[Hyperimmunoglobulinemia E, recurring staphylococcal infections and a defect in granulocyte chemotaxis in adults. A variant of Job's syndrome]. 404 79

Effects of lithium carbonate on peripheral white blood cell and granulocyte counts were investigated in children treated for acute lymphoblastic leukaemia and non-Hodgkin malignant lymphoma. Li2CO3 given orally for two weeks in a single daily dose of 700 mg/m2 caused a significant and lasting increase in the peripheral WBC and granulocyte counts and increased the granulocyte ratio during induction of remission and maintenance cytotoxic therapy. Haematologic actions and the long-term effect of lithium carbonate are discussed.
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PMID:Effect of lithium carbonate on the peripheral leukocyte count in children suffering from haematological malignancies. 641 73

This work was performed with L 428, a cell line established in 1978 from a patient with Hodgkin's disease. These in vitro cells represent counterparts of in vivo Hodgkin and Sternberg-Reed cells. L 428 and its derived sublines produce a significant amount of colony-stimulating factor (CSF) compared to standard preparations of CSF (fetal liver conditioned medium). Hodgkin-cell-derived conditioned medium, tested in cord-blood assays and in semi-solid agar systems, induced myeloproliferation predominantly. Production of CSF is independent of fetal calf serum concentration in the cultures. L 428-conditioned medium could provide an excellent source for characterization and purification of granulocyte CSF.
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PMID:Production of colony-stimulating factors by Hodgkin cell lines. 660 Jul 21

To clarify the origin of Hodgkin (H) and Sternberg-Reed (SR) cells, frozen sections of lymph nodes from 30 patients with Hodgkin's disease were immunostained with a large panel of monoclonal antibodies reactive with cells of lymphoid tissue and granulopoiesis. The results showed that: (a) H and SR cells are devoid of markers specific to, or characteristic of B cells, macrophages, dendritic reticulum cells, interdigitating cells, or cells of erythropoietic or thrombopoietic origin; (b) the vast majority of H and SR cells contain granulocyte-related antigens detectable with the monoclonal antibodies TU9 and 3C4, but constantly lack other granulocytic cell markers (such as peroxidase and chloroacetate esterase). Monoclonal antibodies raised against a Hodgkin's disease-derived cell line included one, Ki-1, that was found to be selectively reactive with H and SR cells and a minute, but distinct cell population in normal lymphoid tissue and bone marrow. The latter, as yet unidentified cell population appears to be the normal equivalent of H and SR cells.
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PMID:Evidence for the detection of the normal counterpart of Hodgkin and Sternberg-Reed cells. 667 60

Opsonic and antibody responses to pneumococcal polysaccharide types 6A, 19F and 23F were evaluated before and after vaccination with a 14-valent pneumococcal vaccine in 25 patients splenectomized due to trauma, non-malignant or malignant disease and in 8 non-splenectomized patients with malignant disease. In approximately 50% of the tests, a 2-fold or greater increase in antibody concentrations and a significantly enhanced opsonization of pneumococci was found. A close correlation between antibody increase an enhancement of opsonization was demonstrated. 93% of paired samples with postimmunization antibody increase above 150 ELISA units showed significantly enhanced opsonization. Increased postvaccination opsonic activity and antibody levels were infrequently accompanied by increased granulocyte chemotactic activity of the serum. No significant difference in antibody and opsonic response to vaccination was found between the groups of patients, except for patients with Hodgkin's disease receiving chemotherapy, who had a reduced immunization response. Prevaccination antibody concentration, type of antigen or age of the patients did not influence the outcome of vaccination.
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PMID:Opsonic and antibody responses to pneumococcal polysaccharide types 6A, 19F and 23F after vaccination of immunocompromised patients. 674 Feb 47

In this study the antigenic profile of Hodgkin (H) and Sternberg-Reed (SR) cells from cases of Hodgkin's disease was analysed using a large panel of monoclonal and polyclonal antibodies reactive with cells of lymphoid and haemotopoietic origin. The aim of this investigation was, firstly, to throw light on the origin of H and SR cells and, secondly, to determine whether there is any evidence to support recent suggestions that H and SR cells differ antigenically between different histological categories of Hodgkin's disease. Frozen sections (from 24 cases) and paraffin sections (83 cases) were stained by immunoenzymatic methods and the results compared with those obtained from staining a wide variety of reactive and neoplastic tissue samples (including examples of tuberculosis, sarcoidosis, malignant histiocytosis, histiocytosis X, osteomyelosclerosis and non-Hodgkin's lymphoma). The results revealed that H and SR cells of all types of Hodgkin's disease consistently lack markers found on null cells, B cells, T cells, cells of monocyte/macrophage series, interdigitating reticulum cells, dendritic reticulum cells and erythropoietic and thrombopoietic cells. However, H and SR cells constantly expressed an antigen detectable with the recently produced monoclonal antibody Ki-I. The vast majority of typical and lacunar type H and SR cells contained the granulocyte-related antigens detected by monoclonal antibodies TU5, TU6, TU9 and 3C4, whereas other more or less specific granulopoietic cell markers (such as peroxidase, chloroacetate esterade, lysozyme, cationic leukocyte antigen and OKMI) were consistently absent. H and SR cells in cases of nodular paragranuloma (nodular type of Hodgkin's disease with lymphocyte predominance) were not monotypic in light chain type (as has been previously reported), but rather contained chi and lambda chains within the same cells, as do typical and lacunar type H and SR cells. Immunostaining of normal and hyperplastic lymphoid tissue with the Ki-I antibody led to the detection of a new, as yet unidentified, small-cell population of unknown origin and function, which is present between, around, and within cortical follicles. It is concluded from these findings that H and SR cells constitute a unique cell type that differs in many properties from all other known cell types. Furthermore, H and SR cells of the various histological types of Hodgkin's disease are more closely related than previously believed. It is suggested that the hitherto unknown cell population detected with the monoclonal antibody Ki-I in normal lymphoid tissue is the normal equivalent of H and SR cells.
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PMID:Identification of Hodgkin and Sternberg-reed cells as a unique cell type derived from a newly-detected small-cell population. 675 30

To clarify the origin of Hodgkin (H) and Sternberg-Reed (SR) cells, frozen sections of lymph nodes from 25 patients with Hodgkin's disease were immunostained with a large panel of monoclonal antibodies reactive with cells of lymphoid tissue and granulopoiesis. The results showed that (a) H and SR cells are devoid of markers specific to, or characteristic of B cells, macrophages, dendritic reticulum cells, or interdigitating reticulum cells, and (b) the vast majority of H and SR cells contain granulocyte-related antigens detectable with the monoclonal antibodies TU9 and 3C4, but constantly lack other granulocytic cell markers (such as peroxidase and chloroacetate esterase). Monoclonal antibodies raised against a Hodgkin's disease-derived cell line included one, Ki-l, that was found to be selectively reactive with H and SR cells and a minute, but distinct, cell population in normal lymphoid tissue and bone marrow. The latter hitherto unknown cell population appears to be the normal equivalent of H and SR cells.
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PMID:Evidence for the origin of Hodgkin and Sternberg-Reed cells from a newly detected small cell population. 686 7

An overdose of CCNU (600 mg over a 15-d period) was unintentionally ingested by a patient with advanced Hodgkin's disease subjected to combination chemotherapy. A severe bone marrow depression occurred 3 weeks after the start of the CCNU treatment. The nadir of the platelet count was reached after 4 weeks and that of the granulocyte count after 5 weeks. At the nadir of the white blood cell count, colony-forming cells (CFU-C) were found in significantly reduced numbers in the bone marrow, and were not found at all in the peripheral blood; the amount of colony-stimulating activity (CSA) produced by peripheral blood cells was reduced. However, the cells producing CSA recovered earlier than the CFU-C, and the CSA peak value was reached about 1 week before the peak value for CFU-C in the bone marrow. Thus, in vivo CSA-producing cells appeared to be more resistant to CCNU than were CFU-C, and their recovery appeared to be a prerequisite for the recovery of CFU-C and myelopoietic cells.
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PMID:CCNU toxicity after an overdose in a patient with Hodgkin's disease. Effects on colony-forming cells (CFU-C) and colony-stimulating activity (CSA). 686 12


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